Ma. Heneghan et al., ACTIVATED PROTEIN-C RESISTANCE, THROMBOPHILIA, AND INFLAMMATORY BOWEL-DISEASE, Digestive diseases and sciences, 43(6), 1998, pp. 1356-1361
Thromboembolic events frequently complicate the clinical course of pat
ients with inflammatory bowel disease (IBD). Hereditary thrombophilia
may contribute to this tendency. Resistance to activated protein C is
the most recently described thrombophilic state and may account for up
to 40% of patients with thrombophilia. Thirty-seven patients with IBD
were studied (mean age 44 years, range 18-82 years). Three patients h
ad a history of thrombotic episodes, The 37 controls included 23 men a
nd 17 women (mean age 48 years, range 16-89 years). Disease activity w
as assessed using the Harvey Bradshaw index for patients with Crohn's
disease and the Truelove and Witts grading system for patients with ul
cerative colitis. Levels of fibrinogen, antithrombin III (ATIII), prot
ein C, protein S, activated protein C resistance (APCR), and the prese
nce of a lupus anticoagulant (LA) were determined. Median ATIII levels
in patients with IBD were significantly lower than controls (98% vs 1
06%, P = 0.007), while fibrinogen was elevated (4.2 vs 3.3 g/liter, P
= 0.026) despite quiescent disease activity. LA was detected in 7/37 p
atients in the IBD group compared to 0/37 controls. (chi(2) = 5.68, P
= 0.017). NO Significant difference was observed in levels of inherite
d thrombophilic factors and in particular APCR between IBD patients an
d controls. In conclusion, the presence of inherited thrombophilic def
ects, in particular APCR, is uncommon in patients with PBD and does no
t merit routine screening.